You are on page 1of 8

Etsubdink Mulugeta ID 011/14

Anesthesia management for patient with DM


 Diabetes mellitus (DM) is defined as a hetrogeneous metabolic disorder
characterized by common feature of chronic hyperglycaemia with disturbance of
carbohydrate,fat and protein metabolism.

Classification

Four broad types

 Type 1 diabetes mellitus


 Type 2 diabetes mellitus
 Gestational Diabetes Mellitus (GDM)
 Other specific types of DM

Type 1 diabetes mellitus

 Juvenile diabetes
 5% to 10% of all DM
 Abrupt onset of the disease
 Caused by T cell–mediated autoimmune destruction of beta cells
 Resulting in complete absence or minimal circulating levels of insulin Require
Insulin therapy
 Cause unknown

Type 2 diabetes mellitus

 80% to 90% of all cases of DM


 Typically in the middle to older age group and are obese
 The milder form can occur in young people
 Gradual onset of the disease Characterized by relative beta cell insufficiency and
insulin resistance
 May have normal or elevated levels of insulin

Gestational Diabetes Mellitus (GDM)


 DM diagnosed in the third trimester of pregnancy that was not clearly overt
diabetes prior to gestation.

Diagnostic criteria

24-28 weeks, without previous DM diagnosis

FBG ≥ 92 mg/dl (5.1 mmol/l

1 hour BG: ≥ 180 mg/dl (10.0 mmol/l

2 hour BG: ≥ 153 mg/dl (8.5 mmol/l

Other specific types of DM

Types of DM with various etiologies

 Monogenic diabetes syndromes (such as neonatal diabetes and maturity-onset


diabetes of the young [MODY]
 Diseases of the exocrine pancreas
 Other endocrinopathies
 Pancreatic dysfunction caused by drugs, chemicals or infections.

Clinical Features

Polyuria Blurry vision

Polydipsia Headache

Polyphagia Fatigue

Slow healing of cuts Itchy skin

Diagnosis of DM Prediabetes

 FPG 100 mg/dL (5.6 mmol/L) to 125 mg/dL (6.9 mmol/L) OR


 2-h PG during 75-g OGTT 140 mg/dL (7.8 mmol/L) to 199 mg/dL (11.0 mmol/L)
OR
 A1C 5.7–6.4% (39–47 mmol/mol)
Criteria for the diagnosis of diabetes

 Fasting plasma glucose ≥126 mg/dL (7 mmol/L) or


 Two-hour plasma glucose ≥200 mg/dL (11.1 mmol/L) OGTT or
 A1C ≥6.5%(48 mmol/mol) or
 In a patient with classic symptoms of hyperglycemia or hyperglycemic crisis, RBS
≥200 mg/dL (11.1 mmol/L).

Complication

Acute and chronic

Acute

 Diabetic ketoacidosis (DKA)


 Hyperosmolar non ketotic coma (HONC)
 Hypoglycemia

Chronic

Microvascular Macrovascular

Nephropathy Coronary artery disease

Neuropathy Cerebrovascular accidents

Eye disease Peripheral vascular disease Encephalopathy

Management of DM

The major components of the treatment of diabetes are:

 Diet control
 Exercise
 Oral hypoglycemic agent
 Insulin therapy

Oral hypoglycemic agent

Biguanides
Metformin first recommended

 Pharmacologic agent for type 2 DM Decreases hepatic glucose output


 Enhances the sensitivity of both hepatic and peripheral tissues to insulin.
 Antilipolytic effect ↓FFA and TGs leads to ↓gluconeogenesis .
 Inhibits intestine glucose absorption

Sulfonylureas

1st generation

Tolbutamide Acetohexamide Tolazamide Chloropamide

2nd generation

Glyburide Glipizide

 Lower serum glucose by increasing insulin secretion.


 They are a second line of choice in T2 DM.
 For patients with any renal impairment, glipizide is preferred.
 Severe hypoglycemia can occur in patients with significant renal impairment.

Glucagon-like peptide-1 agonists

 It enhances insulin secretion


 Suppresses glucagon release
 Delays gastric emptying, and suppresses appetite. Decrease fasting and postprandial
glucose concentrations, HbA1C by 1–2%, and weight by 25 kg.
 GI side-effects: nausea, vomiting, and diarrhoea

Dipeptidyl peptidase-4 inhibitors

 They enhance the effects of endogenous GLP-1 by inhibiting the action of DPP-4.
 Saxagliptin, sitagliptin, and vildagliptin are currently available.
 Can be used as monotherapy,low risk of hypoglycaemia, and less GI side-effects
than the GLP-1 agonists.

Thiazolidinediones(TZD)
 Reduce insulin resistance and improve sensitivity to insulin in muscle.

Rosiglitazone

Pioglitazone are most commonly used

 They do not cause hypoglycemia


 They are third tier agents.
 Are associated with significant weight gain.
 Increased risk of congestive heart failure (CHF) Associated with fluid retention and
peripheral edema 15%.
 Pioglitazone has been associated with an increased risk of bladder cancer.

Alpha-glucosidase inhibitors

 Slow the digestion of ingested carbohydrates


 Delay glucose absorption into the bloodstream
 Decrease postprandial blood glucose levels
 Abdominal pain, flatulence, and diarrhea are common.
 These effects usually diminish over time (4-8 weeks).

Acarbose

Miglitol

INSULIN THERAPY

 Short acting (crystalline| regular).


 Intermediate-acting insulin ( NPH or Lente)
 Long acting insulin(ultra lente PZI) & Long acting (NPH ,Isophane).

Anesthesia management for Diabetes mellitus

Anesthetic management should include:

 preoperative
 Intraoperative
 Postoperative

Peri-operative goal

 Maintain blood glucose level between 120-180mg/dl.


 Reflex release of catecholamine that produces sympathetic over activity may
misinterpreted as light anesthesia.

Preoperative Evaluation

 Determining end-organ complications of DM. recent ECG, blood urea nitrogen,


potassium, creatinine, glucose, and urinalysis.
 Determining the patient’s glucose-lowering regimen. Patients may be on different
types of insulin regimens and oral hypoglycemic agents. Preoperative counseling
has to be specific to the patient’s glucoselowering regimen.
 Determine patient glycemic control and the need for preoperative intervention to
control glucose levels.
 Evaluation includes assessment for possible cardiac and renal disease, control of
hypertension, and examination for limited joint mobility (especially neck) that may
affect endotracheal intubation.
 Prior anesthetic records should be reviewed to determine whether difficulties with
intubation or perioperative diabetic complications were documented previously.
 Recommended to postpone nonurgent or elective surgery if there is an acute rise in
glucose to above 400 mg/dL

Management of Insulin in the Preoperative Period Based on;-

 Type of operative procedure(minor/major)


 IDDM/NIDDM
 Poorly controlled or well controlled

Intraoperative Management

 The goal of intraoperative blood glucose management is to avoid hypoglycemia


 If intra operative administration of glucose is needed
 Intermittent infusion
 Continuous infusion

Intermittent

 Begin an infusion of glucose (5-10gm/hr) and k(2-4meq/hr)


 Measure blood glucose every 1-2 hrs during surgery and during early post
operative period.
 RI (5-10 IU IV) ,bid if blood glucose level is >250 mg/dl.
 Increase rate of IV glucose infusion if the glucose level is <100mg/dl.
 Mix 50 units of RI in 500 ml of NS and initiate IV infusion at 1 unit/hr (10ml/hr).

Continuous infusion

 Regular insulin can be added to normal saline in a concentration of 1 unit/mL and


the infusion begun at 0.1 unit/kg/h or less.
 One unit of regular insulin given to an adult usually lowers plasma glucose by
25–30 mg/dL
 Measure blood glucose level hourly and adjust insulin 150 infusion accordingly.

Fluid management

 Non-dextrose-containing fluid should be used to replace blood loss, urine output,


and third-space or insensible deficits.
 Dextrose is infused only as needed to avoid hypoglycemia and limit protein
catabolism.
 Finally, normothermia is maintained, and postoperative analgesia is provided to
limit excessive stress and resultant antiinsulin effect.
 Avoid hartmans solution.

Infusion of glucose

 Glucose can be infused as 5% DW.


 Treatment of hypoglycemia
 consists of administration of 50 mL of 50% dextrose in water, which typically increases
the serum glucose level by 100 mg/dL.

Post operatively

 NIDDM-stop infusion and restart OH when eating or drinking.


 IDDM-stop infusion when patient resumes eating or drinking and restart sc insulin.

ANESTHETIC DRUGS AFFECT BLOOD SUGAR CONTROL:

 Ketamine: may cause significant hyperglycemia


 Etomidate: blocks adrenal steroidogenesis and hence cortisol synthesis and
decreases the hyperglycemic response to surgery.
 Propofol: The effect of propofol on insulin secretion is not known. Diabetic
patients show a reduced ability to clear lipids from the circulation.
 Halothane, enflurane, isoflurane and sevoflurane: in in vitro studies inhibit the
insulin response to glucose in a reversible and dosedependent manner.
 Benzodiazepines: decrease the secretion of ACTH and the production of cortisol,
when used in high doses.
 They reduce sympathetic stimulation but stimulate growth hormone secretion and
result in a decrease in the glycemic response to surgery. These effects are
minimal when midazolam is given in usual sedative doses.
 Opioids: High-dose opiate anesthetic techniques produce hemodynamic, hormonal
and metabolic stability. However, midazolam and fentanyl may cause
hyperglycemia by reducing glucose clearance.
 B-blockers: The use of b-blockers is associated with slower recovery from
hypoglycemia.

You might also like